Neoangiogenesis is critical for tissue repair in response to injury such as myocardial infarction (MI) or peripheral artery disease. It has been shown that growth factors such as vascular endothelial cell growth factor (VEGF), tumor necrosis factor-alpha (TNF-a), basic fibroblast growth factor (bFGF), or placenta growth factor (PIGF) are potent regulators of angiogenesis. Binding of these angiogenic factors to their receptors may activate a cascade of signaling events including the activation of phosphinositide 3-kinase (PI3K) and mitogen activated protein kinase (MAPK). In response to pro-angiogenic stimuli, vascular endothelial cells (ECs) are activated to migrate to distant sites and proliferate to form new primary capillaries from the pre-existing vascular network (Carmeliet, P., Nat Med, 2000. 6(4): p. 389-95; Cross, M. J. and L. Claesson-Welsh, Trends Pharmacol Sci, 2001. 22(4): p. 201-7; Ferrara, N., Kidney Int, 1999. 56(3): p. 794-814; Folkman, J. and Y. Shing, J Biol Chem, 1992. 267(16): p. 10931-4; Maglione, D., et al., Proc Natl Acad Sci USA, 1991. 88(20): p. 9267-71; Maglione, D., et al., Oncogene, 1993. 8(4): p. 925-31; Risau, W., Nature, 1997. 386(6626): p. 671-4; and Shing, Y., et al., Science, 1984. 223(4642): p. 1296-9). However, despite the importance of ECs in neoangiogenesis, the mechanisms regulating this process remain poorly understood.